Lung transplantation is lifesaving for patients with end-stage lung diseases. However, its long-term success continues to be challenged by chronic lung allograft dysfunction (CLAD) despite the improvement of the early survival1. CLAD, mainly recognized as bronchiolitis obliterans syndrome (BOS), is a major cause of morbidity and mortality in long-term survivors. CLAD affects about 50% of lung transplant recipients 5 years after lung transplantation1. No effective treatment has yet been established.
Recently, restrictive allograft syndrome (RAS) has been identified as a novel subtype of CLAD10,11. Since RAS and BOS (CLAD without RAS) show distinct clinical, radiological and pathological manifestations, it is suggested that development of these CLAD subtypes may involve distinct molecular pathways.
U.S. Pat. No. 8,247,175 (Keshavjee et al), describes that IL-6/IL-10 ratio measured in the donor lung before implantation significantly predicted recipient 30 day primary graft failure.
A differential proteomic analysis of BAL fluid from a small group of lung transplant patients with or without chronic graft dysfunction RAS subtype identified 30 proteins that were not present in BAL from non-CGD samples (18).